18 research outputs found
Suivi des introgressions dans les croisements interspécifiques chez le riz: utilisation des marqueurs moléculaires
La diversité génétique des espèces sauvages de riz est d'un grand intérêt en amélioration des plantes. Malgré de fortes barrières reproductives, des hybrides interspécifiques peuvent être obtenus grâce à la récupération des embryons par culture #in vitro et être recroisés ensuite pour introduire des caractères utiles dans les riz cultivés. Au fur et à mesure que la carte de liaison génétique RFLP (polymorphisme de longueur de fragment de restriction) devient de plus en plus saturée, les marqueurs moléculaires constituent un nouvel outil puissant pour analyser et comprendre les mécanismes de la recombinaison dans les croisements éloignés. Trois exemples d'application des marqueurs moléculaires au suivi des introgressions sont présentés à partir d'activités développées à l'ORSTOM (Institut Français de Recherche Scientifique pour le Développement en Coopération) de Montpellier ou de collaborations avec l'IRRI (Institut International de Recherche sur le Riz, Philippines) et l'Université Cornell (Etats-Unis). Ils concernent l'analyse de générations précoces ou de lignées isogéniques développées avec des espèces sauvages de riz possédant le même génome que le riz cultivé (#O. longistaminata) ou des génomes cytogénétiquement différents (#O. brachyantha, génome F) et (#O. australiensis, génome E). (Résumé d'auteur
Influenza vaccination during the first 6 months after solid organ transplantation is efficacious and safe
Preventing influenza infection early after transplantation is essential, given the disease's high mortality. A multicentre prospective cohort study in adult solid organ transplant recipients (SOTR) receiving the influenza vaccine during four consecutive influenza seasons (2009-2013) was performed to assess the immunogenicity and safety of influenza vaccination in SOTR before and 6 months after transplantation. A total of 798 SOTR, 130 of them vaccinated within 6 months of transplantation and 668 of them vaccinated more than 6 months since transplantation. Seroprotection was similar in both groups: 73.1% vs. 76.5% for A/(H1N1) pdm (p 0.49), 67.5% vs. 74.1% for A/H3N2 (p 0.17) and 84.2% vs. 85.2% for influenza B (p 0.80), respectively. Geometric mean titres after vaccination did not differ among groups: 117.32 (95% confidence interval (CI) 81.52, 168.83) vs. 87.43 (95% CI 72.87, 104.91) for A/(H1N1) pdm, 120.45 (95% CI 82.17, 176.57) vs. 97.86 (95% CI 81.34, 117.44) for A/H3N2 and 143.32 (95% CI 103.46, 198.53) vs. 145.54 (95% CI 122.35, 174.24) for influenza B, respectively. After adjusting for confounding factors, time since transplantation was not associated with response to vaccination. No cases of rejection or severe adverse events were detected in patients vaccinated within the first 6 months after transplantation. In conclusion, influenza vaccination within the first 6 months after transplantation is as safe and immunogenic as vaccination thereafter. Thus, administration of the influenza vaccine can be recommended as soon as 1 month after transplantation. Clinical Microbiology and Infection (C) 2015 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved
IFNγ triggers a LIGHT-dependent selective death of motoneurons contributing to the non-cell-autonomous effects of mutant SOD1
Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease that primarily affects motoneurons in the brain and spinal cord. Dominant mutations in superoxide dismutase-1 (SOD1) cause a familial form of ALS. Mutant SOD1-damaged glial cells contribute to ALS pathogenesis by releasing neurotoxic factors, but the mechanistic basis of the motoneuron-specific elimination is poorly understood. Here, we describe a motoneuron-selective death pathway triggered by activation of lymphotoxin-β receptor (LT-βR) by LIGHT, and operating by a novel signaling scheme. We show that astrocytes expressing mutant SOD1 mediate the selective death of motoneurons through the proinflammatory cytokine interferon-γ (IFNγ), which activates the LIGHT-LT-βR death pathway. The expression of LIGHT and LT-βR by motoneurons in vivo correlates with the preferential expression of IFNγ by motoneurons and astrocytes at disease onset and symptomatic stage in ALS mice. Importantly, the genetic ablation of Light in an ALS mouse model retards progression, but not onset, of the disease and increases lifespan. We propose that IFNγ contributes to a cross-talk between motoneurons and astrocytes causing the selective loss of some motoneurons following activation of the LIGHT-induced death pathway